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Biomedical subjects

M Yamamura

Publications and source records attributed to M Yamamura.

At least 235 records · Page 13Linked to original sources
PubMed1988

A behavioral pharmacological study of mafoprazine, a new phenylpiperazine derivative.

Behavioral pharmacological studies on mafoprazine, a new drug for the prevention of aggressive behavior, were performed to compare its effects with those of an existing drug, azaperone (Stresnil). The acute toxicity of mafoprazine in mice was slightly stronger than that of azaperone. Mafoprazine showed the following effects (at 0.2 to 2.0 mg/kg, s.c.): a decrease in spontaneous motor activity, prolongation of the duration of pentobarbital anesthesia, inhibition of long-term isolation-induced aggressive behavior, inhibition of olfactory bulbectomy-induced hyperemotionality and muricide behavior in mice and rats, and a marked taming and tranquilizing effect on aggressive behavior in dogs. These effects of mafoprazine were qualitatively the same as those of azaperone. Mafoprazine showed cataleptogenicity in rats at 5 mg/kg, s.c. or more and motor incoordination in rats at 0.2 mg/kg, s.c. or more. In the experiment on operant behavior in rats, the effect of mafoprazine on differential reinforcement of the low rate (DRL) response was almost the same as those of azaperone and chlorpromazine. These results indicate that mafoprazine has substantially the same psychotropic effect as azaperone, while the former has a weaker action on the extrapyramidal system than the latter, suggesting that mafoprazine could be used as a unique aggression-inhibiting drug.

Aggression↗
PubMed1988

[A case report of brain metastasis due to an advanced gastric cancer].

In April 1984, a 49-year-old male underwent a partial gastrectomy for advanced gastric cancer. At that time, many metastatic foci were found, for example, in the rib, the lumbar vertebrae, the cervical vertebrae, and in the abdominal lymph nodes. Approximately one year later, he suddenly became disturbed and lost consciousness. A metastatic brain tumor was diagnosed. To destroy this tumor the patient received a course of irradiation therapy with a total dose of 45 gys directed toward head. Several months later, however, recurrence of the tumor was detected at the same intracranial region. Thus, a course of therapy, employing a combination of FT-207 and ACNU, was initiated against the recurrent tumor. Though the tumor was not eliminated, the patient manifested few of the prior symptoms. This state has continued for several months, with the patient having survived for three years after his gastrectomy. The following report will present the details of this case.

Brain Neoplasms↗
PubMed1988

Effect of alpha-1-antichymotrypsin on activity of DNA primase isolated from human stomach adenocarcinoma cells.

This paper describes an investigation into the effect of alpha-1-antichymotrypsin (ACT) on DNA primase. DNA primase was partially purified from human stomach carcinoma cells. It was found that poly(dC)-dependent DNa primase activity was inhibited by ACT and the inhibition was proportional to the concentration of the inhibitor. The inhibitory effect of ACT remained even after ACT lost most of its chymotrypsin-inhibitory activity by heat treatment. Poly(dT)-dependent primase activity was enhanced by the presence of ACT. The enhancement was effective up to a concentration of 1mg/ml.

Adenocarcinoma↗
PubMed1988

Incorporation of alpha-1-antichymotrypsin into human stomach adenocarcinoma cell nuclei and inhibition of DNA primase activity.

Incorporation of alpha-1-antichymotrypsin (ACT) into human stomach adenocarcinoma cell nuclei and the effect of ACT on DNA primase from the same carcinoma cells were studied. ACT or [125I]-ACT were observed in carcinoma cell nuclei and high specific radioactivity was detected in washed nuclear fraction when 0.4 mg of ACT or [125I] ACT (8 x 10(7) cpm) was intravenously injected into carcinoma bearing nude mice 2 h before killing. The molecular weight of radioactivity presented in cell nuclei was same as the intact ACT on SDS-polyacrylamide gel electrophoresis. ACT inhibited DNA primase activity and this inhibiting activity was stable than its chymotrypsin inhibiting activity. The results presented here show ACT is incorporated into carcinoma cell nuclei without modification of its molecular weight and may inhibit DNA primase activity.

Adenocarcinoma↗
PubMed1988

Alpha-1-antichymotrypsin (ACT) as an immune regulatory agent.

This study was carried out to elucidate the interaction of alpha-1-antichymotrypsin (ACT) with the immune reaction induced by interleukin-2 (IL-2). ACT, isolated from human sera and determined to be a single glycoprotein, was added to human peripheral T-cell cultured with IL-2. It was found that ACT effectively suppressed T-cell activation induced by IL-2, but the suppressive effect of ACT was inversely proportional to the concentration of IL-2. A similar effect was found when T-cells were stimulated with PHA. ACT had a suppressive effect when suboptimal concentrations of PHA were used, however this suppressive effect could not be found at the optimal PHA concentration. These findings suggest that ACT may be a regulatory agent in immune reactivity where low concentrations of IL-2 are present. Even under normal conditions, an individual is surrounded and invaded by numerous foreign elements and it may be that small amounts of IL-2 are constantly produced, which would indefinitely trigger chained immune reactions if there were no regulatory agent like ACT.

Adjuvants, Immunologic↗
PubMed1988

Binding of modified alpha-1-antichymotrypsin to mitogen-stimulated human lymphocyte membrane: a model for immune suppression.

Alpha-1-antichymotrypsin (ACT), an acute phase reactant protein elevated during acute inflammation, and its derivatives (asialo ACT and acid-exposed asialo ACT) were investigated their effect on lymphocyte proliferative responses, and evidence for binding to lymphocyte membranes as well as the characteristics of this binding were investigated. Acid-exposed asialo ACT significantly reduced 3H-thymidine incorporation into human peripheral lymphocytes stimulated by phytohemagglutinin (PHA) though native ACT could not inhibit the mitogen-induced lymphoproliferation and asialo ACT moderately inhibited it. In order to determine the interaction of ACT and its derivatives to lymphocyte membranes, the binding of 125I-labelled ACT and its derivatives to membranes of intact lymphocyte and extracted lymphocyte membranes was examined. The binding of 125I-labelled native ACT and asialo ACT to resting and PHA-stimulated lymphocyte membrane was low. And the binding of 125I-labelled acid-exposed asialo ACT to resting lymphocyte membrane was also low. However, when lymphocytes were stimulated by mitogens the binding of 125I-labelled acid-exposed asialo ACT increased significantly. The binding of 125I-labelled acid-exposed asialo ACT to the membrane extracted from PHA-stimulated lymphocytes was time-dependent and saturation was reached at 120 min at 37 degrees C. One mg of membrane could bind a maximum of approximately 83 pmol of acid-exposed asialo ACT with dissociation constant of 0.73 microM. Other unlabelled serum glycoproteins such alpha-1-antitrypsin, alpha-1-acid glycoprotein, transferrin, and proteinase inhibitors including chymostatin, leupeptin and soy bean trypsin inhibitor did not compete with 125I-labelled acid-exposed asialo ACT for binding sites in simultaneous competition assays.

Cell Membrane↗
PubMed1987

Dog erythrocyte rosette-forming lymphocyte: blockage by OKT11 monoclonal antibody.

Human peripheral blood mononuclear cells (PBM) were separated into sheep erythrocyte rosette-forming (Es+) and non Es+ cells by the Ficoll-Hypaque gradient sedimentation method. Thirty-eight percent of the Es+ cells formed rosettes with dog erythrocytes and were designated as Es+Ed+ cells. The remaining Es+ cells were designated as Es+Ed- cells. Only a few non Es+ cells formed rosettes with dog erythrocytes. Among Es+Ed+ cells, T4 antigen-positive cells were observed approximately 1.7 times as often as T8 antigen-positive cells, when measured by staining with OKT4 or OKT8 monoclonal antibody. Among Es+Ed- cells, however, T4 and T8 antigen-positive cells were observed in almost equal proportion. Preincubation of PBM with OKT11 monoclonal antibody, but not with OKT4 monoclonal antibody, inhibited the rosette formation with dog as well as sheep erythrocytes. These results indicated that Es+Ed+ cells were a subpopulation of T-cells in which a majority of the cells were T4 antigen-positive, and that the binding sites of dog erythrocytes on human T-cells was closely linked with that of sheep erythrocytes.

Animals↗
PubMed1987

[A case report of triple cancer (lung, stomach & liver cancer)--with special reference to operable cases reported in the literature].

A case of a triple cancer in the lung, stomach, and liver has been experienced and a subsequent operation was performed. It has been noted that the occurrence of triple cancers have increased by about four times during the last decade, no doubt due to progress in more accurate diagnoses and from therapeutic effects. However, operations involving triple cancer still are rare and such cases in the literatures are discussed.

Adenocarcinoma↗
PubMed1987

Effect of ethanol on sialidase activity of peripheral lymphocytes.

Sialidase activity of peripheral mononuclear cells, which are mostly lymphocytes, was found to be increased by lectin stimulations in in vitro experiments, but this induction was suppressed in the presence of 50 mM ethanol. This increasing change and its suppressive effect by lectins and ethanol were parallel to blastogenic change of the cells determined by 3H-thymidine uptake. In in vivo, sialidase activity of peripheral MNC prepared from patients with alcoholic liver disease was found to be decreased or not increased in 50% of the cases, in contrast to the marked increase of the activity in non-alcoholic liver diseases observed in our previous study.

Alcoholism↗
PubMed1986

Heat production as a cell cycle monitoring parameter.

A microcalorimetric method was applied to define the cell cycle by measuring heat production of mouse breast cancer cell line, FM3A. FM3A cells, were synchronised at the Go phase and produced 13.0 mu Watts (W) per 1 X 10(6) cells. Although the number of cells in fresh medium remained unchanged during the following 24 hour, a dramatic increase of heat production was observed and maximum heat (46.2 mu W) was produced by the cells at 24 hours when the cell cycle was presumably at the G2 phase. At 26 hours, although cell number increased, heat production decreased. Since the cells were not treated in any manner, this microcalorimetric method of measuring the cell cycle by monitoring heat production can be a very useful tool.

Calorimetry↗